نتایج جستجو برای: kit preparation

تعداد نتایج: 203426  

Journal: :Blood 2003
Koji Hashimoto Itaru Matsumura Tohru Tsujimura Dae-Ki Kim Hideki Ogihara Hirokazu Ikeda Shuji Ueda Masao Mizuki Hiroyuki Sugahara Hirohiko Shibayama Yukihiko Kitamura Yuzuru Kanakura

Substitution of valine (Val) for aspartic acid (Asp) at codon 814 constitutively activates murine c-kit receptor tyrosine kinase (KIT), and Asp816Val mutation, corresponding to murine Asp814Val mutation, is found in patients with mastocytosis and acute myelocytic leukemia. However, the signal transduction pathways responsible for oncogenesis by the Asp814Val mutant (KIT(Val814)) are not fully u...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1998
K Akashi M Kondo I L Weissman

Most mouse thymocytes undergoing positive selection are found on one of two pathways; the c-Kit+ and the c-Kit- pathways. Here, we show that c-Kit and interleukin-7 receptor (IL-7R)-mediated signals support positive selection during the transition from the subpopulation that first expresses cell surface T cell receptor (TCR)-the TCRalpha/betaloCD4(int)/CD8(int) (DPint) c-Kit+ cells to TCRalpha/...

Journal: :Molecular cancer therapeutics 2015
Marianne Le Gall Ronan Crépin Madeline Neiveyans Christian Auclair Yongfeng Fan Yu Zhou James D Marks André Pèlegrin Marie-Alix Poul

KIT is a cell surface tyrosine kinase receptor whose ligand stem cell factor (SCF) triggers homodimerization and activation of downstream effector pathways involved in cell survival, proliferation, homing, or differentiation. KIT-activating mutations are major oncogenic drivers in subsets of acute myeloid leukemia (AML), in mast cell leukemia, and in gastrointestinal stromal tumors (GIST). The ...

Journal: :Slagmark - Tidsskrift for idéhistorie 1970

Journal: :Behavior Analysis in Practice 2013

Journal: :The Journal of Architecture 2020

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2007
Tianhua Guo Narasimhan P Agaram Grace C Wong Glory Hom David D'Adamo Robert G Maki Gary K Schwartz Darren Veach Bayard D Clarkson Samuel Singer Ronald P DeMatteo Peter Besmer Cristina R Antonescu

PURPOSE Resistance is commonly acquired in patients with metastatic gastrointestinal stromal tumor who are treated with imatinib mesylate, often due to the development of secondary mutations in the KIT kinase domain. We sought to investigate the efficacy of second-line tyrosine kinase inhibitors, such as sorafenib, dasatinib, and nilotinib, against the commonly observed imatinib-resistant KIT m...

2015
Xiaoning Gao Ji Lin Li Gao Ailing Deng Xiaolin Lu Yonghui Li Lili Wang Li Yu

The reason that a certain subgroup of acute myeloid leukemia (AML) patients with t(8;21) translocation (generating the AML1/ETO fusion gene) displays a poor survival remains elusive. The proto-oncogene c-kit is expressed in approximately 80% of AML cases. The kinase domain mutation of the c-kit gene, one of the most common gain-of-function mutations associated with t(8;21) AML, predicts higher ...

Journal: :International journal of oncology 2009
Xiaomin Zheng Claudia Oancea Reinhard Henschler Martin Ruthardt

Acute myeloid leukemia (AML) is caused by the cooperation between class I, mostly mutated receptor tyrosine kinases (RTK), and class II oncoproteins, chimeric transcription factors derived from chromosomal translocations. The blasts of 80-90% of AML-patients are positive for the RTK c-Kit. In about 50% of the 'core binding factor' (CBF)-AMLs, c-Kit harbors additional gain-of-function mutations,...

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